This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Elevated intraocular pressure (IOP) is an important risk factor for optic nerve damage in glaucoma. The precise pathophysiological mechanism that leads to RGC death in glaucomatous optic nerve damage by elevated IOP remains unknown. Mitochondrial changes have been involved in the pathophysiology of neuronal death and it is reasonable to speculate that they, too, may cause glaucomatous optic neuropathy. Mitochondrial fission is a cellular response to stress that has an important role in neuronal cell death in neurodegenerative diseases. Our goal is to determine whether elevated hydrostatic pressure induces mitochondrial fission and dysfunction in cultured retinal ganglion cells.